Congestive heart failure (CHF) is a progressive and lethal disease if left untreated. CHF syndrome often evolves as a continuum of clinical adaptations, from the subtle loss of normal function to the presence of symptoms refractory to medical therapy. While the exact etiology of the syndrome that causes heart failure is not fully understood, the primary cause of CHF is left ventricular dysfunction (i.e., the inability of the heart to properly and adequately fill or empty blood from the left ventricle with adequate efficiency to meet the metabolic needs of the body).
In addition, non-cardiac factors can also be activated due the overall degenerative cycle that ensues. These include neuro-hormonal stimulation, endothelial dysfunction, vasoconstriction, and renal sodium retention all of which can cause dyspnea, fatigue and edema rendering patients unable to perform the simplest everyday tasks. These types of non-cardiac factors are secondary to the negative, functional adaptations of the ventricles, cardiac valves and/or load conditions applied to or resisted by these structures. With existing pharmacological, surgical and device-based therapies symptoms can be alleviated, but the quality of a patient's life remains significantly impaired. Further morbidity and mortality associated with the disease is exceptionally high.
Ischemic heart disease is currently the leading cause of CHF in the western world, accounting for greater than 70% of cases worldwide. In these cases, CHF can precipitate from ischemic conditions or from muscle damage (i.e., due to obstruction of a coronary artery) which can weaken the heart muscle, thereby initiating a process known as remodeling in which changes in cardiac anatomy and physiology include ventricular dilatation, regional wall motion abnormalities, decreases in the left ventricular ejection fraction and impairment of other critical parameters of ventricular function. Such left ventricular dysfunction may be further aggravated by hypertension and valvular disease in which a chronic volume or pressure overload can alter the structure and function of the ventricle. Decreases in systolic contraction can lead to cardiomyopathy, which further exacerbates the localized, ischemia damaged tissue or AMI insult into a global impairment, thereby leading to episodes of arrhythmia, progressive pump failure and death.
Ischemia-damaged and/or infarct damaged heart muscle tissue results in progressive softening or degeneration of cardiac tissue. These ischemic and infarcted zones of the heart muscle wall have limited, if not complete loss of tissue contractile functionality and overall physical integrity and present an analogous situation to those presented by vascular aneurysms.
CHF is usually associated with a progressive enlargement of the heart as it increases contractility and heart rate in a compensatory response to the decreasing cardiac output. With this enlargement, the heart's burden is increased to pump more blood with each pump cycle. A phenomenon known as myocardial stretch is implicated in a degenerative cycle/ feedback loop that causes areas of compromised heart muscle tissue to bulge further outward. When the bulging is related to AMI, this behavior is characterized as infarct expansion. With this bulging, the heart's natural contraction mechanism is dissipated and attenuated, resulting in a marked and progressing decrease in cardiac output.
Normal cardiac valve closure (especially that of the mitral valve) is dependent upon the integrity of the myocardium, as well as that of the valve apparatus itself. The normal mitral valve is a complex structure consisting of leaflets, an annulus, chordae tendineae, and papillary muscles. Any damage or impairment in function of any of these key components can render the valve structure incompetent. Impairment of valve function, due to independent factors (i.e., a concomitant valve pathology) or dependent factors (i.e., valve dilation related to dilated cardiomyopathy), can result in valvular insufficiency further exacerbating the degenerative CHF cycle.
The major objectives of heart failure therapy are to decrease symptoms and prolong life. The American Heart Association guidelines suggest that optimal treatment objectives include means to increase survival and exercise capacity, and to improve quality of life, while decreasing symptoms, morbidity and the continued progression of the cardiac degeneration. Various pharmacological and surgical methods have been applied both with palliative and therapeutic outcome goals. However, there still remains no definitive cure for CHF.
Modem pharmacological approaches such as diuretics, vasodilators, and digoxin dramatically lessen CHF symptoms and prolong life by mitigating the non-cardiac factors implicated in the syndrome. Furosemide (more commonly known as Lasix™) is also a valuable diuretic drug which eliminates excess water and salt from the body by altering kidney function and thereby increasing urine output, thus relieving circulatory congestion and the accompanying pulmonary and peripheral edema.
Vasodilators, like angiotensin-converting-enzyme (ACE) inhibitors have become cornerstones in treatment of heart failure. These kinds of vasodilators relax both arterial and venous smooth muscle, thereby reducing the resistance to left ventricular ejection. In patients with enlarged ventricles, the drug increases stroke volume with a reduction in ventricular filling pressure. Administering digoxin has also been found to be positively inotropic (i.e., strengthening to the heart's contractile capability).
On the surgical front, cardiomyoplasty is a recently developed treatment of CHF. In such a procedure, the latissimus dorsi muscle is removed from the patient's shoulder, wrapped around the heart and chronically paced in synchrony with ventricular systole in an effort to assist the heart to pump during systole. The procedure is known to provide some symptomatic improvement, but is controversial with regard to its ability to enable active improvement of cardiac performance. It is hypothesized that the symptomatic improvement is primarily generated by passive constraint and mitigation of the degenerative, remodeling process. In spite of the positive outcome on relieving some of the symptoms, the procedure is highly invasive, requiring access to the heart via a sternotomy, expensive, complex and of unknown durability (due to the muscle wrap blood flow requirements and fibrosis issues).
Another surgical procedure of interest has been developed by R. Bautista, MD. In this procedure, the overall mass, volume and diameter of the heart are physically reduced by dissection and removal of left ventricular tissue. While innovative, the procedure is highly invasive, traumatic and costly. Further, the actual volume reduction results in a reduction in valve competence and elicits the associated regurgitation.
Surgical treatment of valvular dysfunction includes a wide range of open procedure options ranging from mitral ring annuloplasty to complete valve replacement using mechanical or tissue-based valve prosthesis. While being generally successful and routine in surgical practice today, these procedures are also costly, highly invasive and are still have significant associated morbidity and mortality.
More recently, mechanical assist devices which act as a bridge to transplant such as the left ventricular assist device (LVAD) or the total artificial heart (TAH) implant have become available. LVAD's are implantable, mechanical pumps that facilitate the flow of blood from the left ventricle into the aorta. The latest TAH technologies feature many improved design and material enhancements that increase their durability and reliability. Still, the use of such devices is limited by high costs and a lack of substantial, clinical evidence warranting their use.
Other device-based options for CHF patients include approaches for reshaping, reinforcement and/or reduction of the heart's anatomical structure using polymeric and metallic bands, cuffs, jackets, balloon/balloon-like structures or socks to provide external stress relief to the heart and to reduce the . propensity/capability of the cardiac tissue to distend or become continually stretched and progressively damaged with pump cycles. Examples of such devices are U.S. Pat. No. 2002/0045799 and U.S. Pat. No. 5,702,343. In addition, devices are being studied that attempt to prevent the tissue remodeling using tethers and growth limiting struts or structures described in various patents (i.e., U.S. Pat. No. 6,406,420).
Generally, all of these concepts support the cardiac muscle and restrict growth externally and globally via surgical placement about the epicardium and in some instances are positioned across the cardiac muscle tissue. As a result, these types of approaches require unnecessary positioning of the devices over healthy (non local, undamaged) areas or zones of the heart affecting the entire organ when the primary treatment is usually focused is on the left ventricle or the mitral valve annulus. Such non-localized treatment can elicit iatrogenic conditions such as undesired valvular dysfunction and/or constrictive physiology due to over restriction of the heart by such restraints.
Recently, several-device based options have been introduced where implants are positioned by minimally invasive means in the coronary sinus in one configuration and then assume a post deployment configuration that constricts around the heart annulus to improve valve competence in dilated cardiomyopathy (see, U.S. patent application Publication No. 2002/016628.) While appealing, the clinical efficacy of this approach is unknown at this time.
The ultimate treatment for people suffering end stage CHF is a heart transplant. Transplants represent a massive challenge with donor hearts generally in short supply and with the transplant surgery itself presenting a high risk, traumatic and costly procedure. In spite of this, transplants present a valuable, albeit limited, upside, increasing life expectancy of end stage congestive heart failure patient from less than one year up to a potential five years.
In view of the above, it should be evident that there is currently no ideal treatment among the various surgical, pharmacological, and device-based approaches to treat the multiple cardiac and non-cardiac factors implicated with the syndrome of CHF. Accordingly, there is a clear, unmet clinical need for technology that is minimally invasive (especially, percutaneous) that can prevent, treat or reduce the structural remodeling to the heart and its sub-structures across the continuum of the CHF syndrome beginning acutely with the ischemia or ischemic infarct through the end stages where there is often left ventricular and valvular dysfunction refractory to conventional treatments.
Still, patients suffering from CHF, who are unresponsive to medication, generally precluded to open surgical approaches and potentially awaiting transplant could derive massive and direct benefit from a minimally invasive device as provided by the present invention to limit further degeneration of their condition. In addition, implant embodiments of the present invention can also facilitate positive or reverse remodeling (i.e., provide a mild compressive force both during systole and diastole to improve cardiac output and efficiency).